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Cells
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The Role of Cellular Senescence in Health, Disease, and Aging
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The Role of Cellular Senescence in Health, Disease, and Aging

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 2833

Special Issue Editor

Dr. Yasumichi Inoue

E-Mail Website
Guest Editor
Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan
Interests: cancer; cell cycle; cellular senescence; endoplasmic reticulum stress; molecular target drugs; p53; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As the human population ages, people are faced with various health challenges brought on by old age. The concept of the senescence of an individual is also gaining acceptance as a result of the greater understanding of the senescence of the cells that make up the organism. Senescence research has been a very active field in recent years, as the role of aging in disease and physiological processes has become clearer and as aging-based therapeutic interventions have become more promising. In particular, the extension of human life spans via the removal of senescent cells must be seen as an epoch-making event. These groundbreaking matters are produced through the accumulation of deep basic research and the challenge of clinical application on cellular senescence.

This Special Issue provides an open access forum to compile a collection of original research and review articles on the role of cellular senescence in health, disease and aging. We welcome submissions on a wide range of research topics, including molecular mechanisms of cellular senescence and the pathogenesis of diseases such as cancer and age-related diseases caused by cellular senescence.

Dr. Yasumichi Inoue
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • apoptosis
  • cancer
  • cell cycle
  • DNA damage
  • metabolic diseases
  • oxidative stress
  • senolysis
  • senescence
  • therapeutic approach

Published Papers (2 papers)

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Research

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19 pages, 5885 KiB  
Article
GDF15 Modulates the Zoledronic-Acid-Induced Hyperinflammatory Mechanoresponse of Periodontal Ligament Fibroblasts
by Ann Nitzsche, Christoph-Ludwig Hennig, Katrin von Brandenstein, Annika Döding, Ulrike Schulze-Späte, Judit Symmank and Collin Jacobs
Cells 2024, 13(2), 147; https://doi.org/10.3390/cells13020147 - 12 Jan 2024
Viewed by 997
Abstract
Orthodontic tooth movement (OTM) is thought to be impeded by bisphosphonate (BP) therapy, mainly due to increased osteoclast apoptosis and changes in the periodontal ligament (PdL), a connecting tissue between the alveolar bone and teeth. PdL cells, mainly fibroblasts (PdLFs), are crucial regulators [...] Read more.
Orthodontic tooth movement (OTM) is thought to be impeded by bisphosphonate (BP) therapy, mainly due to increased osteoclast apoptosis and changes in the periodontal ligament (PdL), a connecting tissue between the alveolar bone and teeth. PdL cells, mainly fibroblasts (PdLFs), are crucial regulators in OTM by modulating force-induced local inflammatory processes. Recently, we identified the TGF-β/BMP superfamily member GDF15 as an important modulator in OTM, promoting the pro-inflammatory mechanoresponses of PdLFs. The precise impact of the highly potent BP zoledronate (ZOL) on the mechanofunctionality of PdLFs is still under-investigated. Therefore, the aim of this study was to further characterize the ZOL-induced changes in the initial inflammatory mechanoresponse of human PdLFs (hPdLFs) and to further clarify a potential interrelationship with GDF15 signaling. Thus, two-day in vitro treatment with 0.5 µM, 5 µM and 50 µM of ZOL altered the cellular properties of hPdLFs partially in a concentration-dependent manner. In particular, exposure to ZOL decreased their metabolic activity, the proliferation rate, detected using Ki-67 immunofluorescent staining, and survival, analyzed using trypan blue. An increasing occurrence of DNA strand breaks was observed using TUNEL and an activated DNA damage response was demonstrated using H2A.X (phosphoS139) staining. While the osteogenic differentiation of hPdLFs was unaffected by ZOL, increased cellular senescence was observed using enhanced p21Waf1/Cip1/Sdi1 and β-galactosidase staining. In addition, cytokine-encoding genes such as IL6, IL8, COX2 and GDF15, which are associated with a senescence-associated secretory phenotype, were up-regulated by ZOL. Subsequently, this change in the hPdLF phenotype promoted a hyperinflammatory response to applied compressive forces with an increased expression of the pro-inflammatory markers IL1β, IL6 and GDF15, as well as the activation of monocytic THP1 cells. GDF15 appeared to be particularly relevant to these changes, as siRNA-mediated down-regulation balanced these hyperinflammatory responses by reducing IL-1β and IL-6 expression (IL1B p-value < 0.0001; IL6 p-value < 0.001) and secretion (IL-1β p-value < 0.05; IL-6 p-value < 0.001), as well as immune cell activation (p-value < 0.0001). In addition, ZOL-related reduced RANKL/OPG values and inhibited osteoclast activation were enhanced in GDF15-deficient hPdLFs (both p-values < 0.0001; all statistical tests: one-way ANOVA, Tukey’s post hoc test). Thus, GDF15 may become a promising new target in the personalized orthodontic treatment of bisphosphonatepatients. Full article
(This article belongs to the Special Issue The Role of Cellular Senescence in Health, Disease, and Aging)
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Review

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18 pages, 973 KiB  
Review
New Possibilities for Evaluating the Development of Age-Related Pathologies Using the Dynamical Network Biomarkers Theory
by Kazutaka Akagi, Keiichi Koizumi, Makoto Kadowaki, Isao Kitajima and Shigeru Saito
Cells 2023, 12(18), 2297; https://doi.org/10.3390/cells12182297 - 17 Sep 2023
Viewed by 1381
Abstract
Aging is the slowest process in a living organism. During this process, mortality rate increases exponentially due to the accumulation of damage at the cellular level. Cellular senescence is a well-established hallmark of aging, as well as a promising target for preventing aging [...] Read more.
Aging is the slowest process in a living organism. During this process, mortality rate increases exponentially due to the accumulation of damage at the cellular level. Cellular senescence is a well-established hallmark of aging, as well as a promising target for preventing aging and age-related diseases. However, mapping the senescent cells in tissues is extremely challenging, as their low abundance, lack of specific markers, and variability arise from heterogeneity. Hence, methodologies for identifying or predicting the development of senescent cells are necessary for achieving healthy aging. A new wave of bioinformatic methodologies based on mathematics/physics theories have been proposed to be applied to aging biology, which is altering the way we approach our understand of aging. Here, we discuss the dynamical network biomarkers (DNB) theory, which allows for the prediction of state transition in complex systems such as living organisms, as well as usage of Raman spectroscopy that offers a non-invasive and label-free imaging, and provide a perspective on potential applications for the study of aging. Full article
(This article belongs to the Special Issue The Role of Cellular Senescence in Health, Disease, and Aging)
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